To investigate whether SMCs undergo phenotypic modulation in response to factors derived from the pancreatic tumor cells of cachectic pancreatic cancer patients, contractile SMCs were exposed to tumor organoid CM for 72 h and the levels of key contractile proteins (smooth muscle myosin heavy chain (SM-MHC), α-smooth muscle actin (α-SMA), and smooth muscle protein 22-alpha (SM-22α)) were assessed by Western blot. The gene discussed is ACTA1; the disease is familial pancreatic carcinoma.